A growing body of evidence provides new insight into the multifaceted role of TREM2 in regulating the pathological effects provided, in animal AD models and in AD patients, by the extracellular Aβ peptide fibrils [18], the hyperphosphorylation and aggregation of the tau protein [11,19], microgliosis and the ensuing inflammatory reaction [20,21,22,23,24]. The gene discussed is MAPT; the disease is Alzheimer disease.